Abstract 18902: CT Derived Atherosclerotic Plaque Burden and Morphology Are Associated With Impaired Myocardial Blood Flow Using [15O]H2O PET and Fractional Flow Reserve, Independent of Luminal Obstruction
Introduction: Next to coronary lesion severity, atherosclerotic plaque characteristics may influence downstream myocardial perfusion.
Hypothesis: We assessed the hypothesis that quantitative plaque burden and plaque morphology using coronary computed tomography angiography (CCTA) is associated with quantitative myocardial perfusion using [15O]H2O positron emission tomography (PET) as well as invasively derived fractional flow reserve (FFR).
Methods: 208 patients (63% men, age 58 ± 8.7 years) with suspected coronary artery disease were prospectively included. All patients underwent 256-slice CCTA, [15O]H2O PET, and invasive FFR measurements. CCTA derived quantitative plaque burden and morphology were assessed using commercially available software.
Results: Atherosclerotic plaques were present in 179 (86%) patients and 414 of 610 (68%) evaluable coronary arteries. On a per-vessel basis, traditional coronary stenosis indices such as plaque length and volume, minimal lumen area, plaque burden, and stenosis percentage were significantly associated with impaired hyperemic myocardial blood flow (MBF) and FFR. In addition, morphological features such as mixed plaques, positive remodeling (PR), and low attenuation plaque (LAP) also displayed a negative impact on hyperemic MBF and FFR. Multivariable analysis revealed that the morphological feature of PR was independently related to impaired hyperemic MBF as well as an unfavorable FFR (p = 0.004 and p = 0.007, respectively), next to stenosis percentage (p = 0.001 and p < 0.001, respectively), and non-calcified plaque volume (p < 0.001 and p = 0.010, respectively).
Conclusions: In conclusion, positive remodeling and non-calcified plaque volume are associated with detrimental downstream hyperemic myocardial perfusion and FFR, independent from lesion severity.
Author Disclosures: R.S. Driessen: None. W.J. Stuijfzand: None. P.G. Raijmakers: None. I. Danad: None. J.K. Min: None. J.A. Leipsic: None. M.C. Huisman: None. A.A. Lammertsma: None. A.C. Van Rossum: None. N. van Royen: None. P. Knaapen: None.
- © 2016 by American Heart Association, Inc.